Lovastatin Information
Lovastatin () Description
Lovastatin () is a cholesterol lowering agent isolated from a strain of . After oral ingestion, Lovastatin () , which is an inactive lactone, is hydrolyzed to the corresponding β-hydroxyacid form. This is a principal metabolite and an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, which is an early and rate limiting step in the biosynthesis of cholesterol.
Lovastatin () is [1S-[1α(R*),3α,7β,8β(2S*,4S*), 8aβ]]-1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-[2-(tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl)ethyl]-1-naphthalenyl 2-methylbutanoate. The molecular formula of Lovastatin () is C24H36O5 and its molecular weight is 404.54. Its structural formula is:
Lovastatin () is a white, nonhygroscopic crystalline powder that is insoluble in water and sparingly soluble in ethanol, methanol, and acetonitrile.
Each tablet for oral administration, contains 10 mg, 20 mg, or 40 mg of Lovastatin () . In addition, each tablet contains the following inactive ingredients: lactose monohydrate, magnesium stearate, microcrystalline cellulose, and pregelatinized starch. Butylated hydroxyanisole is added as a preservative. The 20 mg tablet also contains D&C Red #30 aluminum lake. The 40 mg tablet also contains D&C Yellow #10 HT aluminum lake.
Lovastatin () Clinical Pharmacology
The involvement of low-density lipoprotein cholesterol (LDL-C) in atherogenesis has been well-documented in clinical and pathological studies, as well as in many animal experiments. Epidemiological and clinical studies have established that high LDL-C and low high-density lipoprotein cholesterol (HDL-C) are both associated with coronary heart disease. However, the risk of developing coronary heart disease is continuous and graded over the range of cholesterol levels and many coronary events do occur in patients with total cholesterol (total-C) and LDL-C in the lower end of this range.
Lovastatin () has been shown to reduce both normal and elevated LDL-C concentrations. LDL is formed from very low-density lipoprotein (VLDL) and is catabolized predominantly by the high affinity LDL receptor. The mechanism of the LDL-lowering effect of Lovastatin () may involve both reduction of VLDL-C concentration, and induction of the LDL receptor, leading to reduced production and/or increased catabolism of LDL-C. Apolipoprotein B also falls substantially during treatment with Lovastatin () . Since each LDL particle contains one molecule of apolipoprotein B, and since little apolipoprotein B is found in other lipoproteins, this strongly suggests that Lovastatin () does not merely cause cholesterol to be lost from LDL, but also reduces the concentration of circulating LDL particles. In addition, Lovastatin () can produce increases of variable magnitude in HDL-C, and modestly reduces VLDL-C and plasma triglycerides (TG) (see Tables I-III under ). The effects of Lovastatin () on Lp(a), fibrinogen, and certain other independent biochemical risk markers for coronary heart disease are unknown.
Lovastatin () is a specific inhibitor of HMG-CoA reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate. The conversion of HMG-CoA to mevalonate is an early step in the biosynthetic pathway for cholesterol.
Lovastatin () Indications And Usage
Therapy with Lovastatin () should be a component of multiple risk factor intervention in those individuals with dyslipidemia at risk for atherosclerotic vascular disease. Lovastatin () should be used in addition to a diet restricted in saturated fat and cholesterol as part of a treatment strategy to lower total-C and LDL-C to target levels when the response to diet and other nonpharmacological measures alone has been inadequate to reduce risk.
- Myocardial infarction
- Unstable angina
- Coronary revascularization procedures
(See , .)
Lovastatin () Contraindications
Hypersensitivity to any component of this medication.
Active liver disease or unexplained persistent elevations of serum transaminases (see ).
Pregnancy And Lactation (see , and ). Atherosclerosis is a chronic process and the discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hypercholesterolemia. Moreover, cholesterol and other products of the cholesterol biosynthesis pathway are essential components for fetal development, including synthesis of steroids and cell membranes. Because of the ability of inhibitors of HMG-CoA reductase such as Lovastatin () to decrease the synthesis of cholesterol and possibly other products of the cholesterol biosynthesis pathway, Lovastatin () is contraindicated during pregnancy and in nursing mothers. Lovastatin () should be administered to women of childbearing age only when such patients are highly unlikely to conceive. If the patient becomes pregnant while taking this drug, Lovastatin () should be discontinued immediately and the patient should be apprised of the potential hazard to the fetus (see , ).
Lovastatin () Warnings
Lovastatin () , like other inhibitors of HMG-CoA reductase, occasionally causes myopathy manifested as muscle pain, tenderness or weakness with creatine kinase (CK) above ten times the upper limit of normal (ULN). Myopathy sometimes takes the form of rhabdomyolysis with or without acute renal failure secondary to myoglobinuria, and rare fatalities have occurred. The risk of myopathy is increased by high levels of HMG-CoA reductase inhibitory activity in plasma.
As with other HMG-CoA reductase inhibitors, the risk of myopathy/rhabdomyolysis is dose related. In a clinical study (EXCEL) in which patients were carefully monitored and some interacting drugs were excluded, there was one case of myopathy among 4933 patients randomized to Lovastatin () 20-40 mg daily for 48 weeks, and 4 among 1649 patients randomized to 80 mg daily.
All patients starting therapy with Lovastatin () , or whose dose of Lovastatin () is being increased, should be advised of the risk of myopathy and told to report promptly any unexplained muscle pain, tenderness or weakness. Lovastatin () therapy should be discontinued immediately if myopathy is diagnosed or suspected. In most cases, muscle symptoms and CK increases resolved when treatment was promptly discontinued. Periodic CK determinations may be considered in patients starting therapy with Lovastatin () or whose dose is being increased, but there is no assurance that such monitoring will prevent myopathy.
Many of the patients who have developed rhabdomyolysis on therapy with Lovastatin () have had complicated medical histories, including renal insufficiency usually as a consequence of long-standing diabetes mellitus. Such patients merit closer monitoring. Therapy with Lovastatin () should be temporarily stopped a few days prior to elective major surgery and when any major medical or surgical condition supervenes.
The risk of myopathy/rhabdomyolysis is increased by concomitant use of Lovastatin () with the following:
Potent Inhibitors Of CYP3A4: Lovastatin () , like several other inhibitors of HMG-CoA reductase, is a substrate of cytochrome P450 3A4 (CYP3A4). When Lovastatin () is used with a potent inhibitor of CYP3A4, elevated plasma levels of HMG-CoA reductase inhibitory activity can increase the risk of myopathy and rhabdomyolysis, particularly with higher doses of Lovastatin () .
The use of Lovastatin () concomitantly with the potent CYP3A4 inhibitors itraconazole, ketoconazole, erythromycin, clarithromycin, telithromycin, HIV protease inhibitors, nefazodone, or large quantities of grapefruit juice (>1 quart daily) should be avoided. Concomitant use of other medicines labeled as having a potent inhibitory effect on CYP3A4 should be avoided unless the benefits of combined therapy outweigh the increased risk. If treatment with itraconazole, ketoconazole, erythromycin, clarithromycin or telithromycin is unavoidable, therapy with Lovastatin () should be suspended during the course of treatment.
Gemfibrozil, Particularly With Higher Doses Of Lovastatin () :The dose of Lovastatin () should not exceed 20 mg daily in patients receiving concomitant medication with gemfibrozil. The combined use of Lovastatin () with gemfibrozil should be avoided, unless the benefits are likely to outweigh the increased risks of this drug combination.
Other Lipid-lowering Drugs (Other Fibrates Or ≥ 1 g/day Of Niacin):The dose of Lovastatin () should not exceed 20 mg daily in patients receiving concomitant medication with other fibrates or ≥ 1 g/day of niacin. Caution should be used when prescribing other fibrates or lipid-lowering doses (≥ 1 g/day) of niacin with Lovastatin () , as these agents can cause myopathy when given alone. The benefit of further alterations in lipid levels by the combined use of Lovastatin () with other fibrates or niacin should be carefully weighed against the potential risks of these combinations.
Cyclosporine Or Danazol, With Higher Doses Of Lovastatin () :The dose of Lovastatin () should not exceed 20 mg daily in patients receiving concomitant medication with cyclosporine or danazol. The benefits of the use of Lovastatin () in patients receiving cyclosporine or danazol should be carefully weighed against the risks of these combinations.
Amiodarone Or Verapamil:The dose of Lovastatin () should not exceed 40 mg daily in patients receiving concomitant medication with amiodarone or verapamil. The combined use of Lovastatin () at doses higher than 40 mg daily with amiodarone or verapamil should be avoided unless the clinical benefit is likely to outweigh the increased risk of myopathy. The risk of myopathy/rhabdomyolysis is increased when either amiodarone or verapamil is used concomitantly with higher doses of a closely related member of the HMG-CoA reductase inhibitor class.
Prescribing recommendations for interacting agents are summarized in Table VI (see also , , ; ).
When the drug was interrupted or discontinued in these patients, the transaminase levels usually fell slowly to pretreatment levels. The increases usually appeared 3 to 12 months after the start of therapy with Lovastatin () , and were not associated with jaundice or other clinical signs or symptoms. There was no evidence of hypersensitivity. In the EXCEL study (see , ), the incidence of persistent increases in serum transaminases over 48 weeks was 0.1% for placebo, 0.1% at 20 mg/day, 0.9% at 40 mg/day, and 1.5% at 80 mg/day in patients on Lovastatin () . However, in post-marketing experience with Lovastatin () , symptomatic liver disease has been reported rarely at all dosages (see ).
In AFCAPS/TexCAPS, the number of participants with consecutive elevations of either alanine aminotransferase (ALT) or aspartate aminotransferase (AST) (> 3 times the upper limit of normal), over a median of 5.1 years of follow-up, was not significantly different between the Lovastatin () and placebo groups (18 [0.6%] vs. 11 [0.3%]). The starting dose of Lovastatin () was 20 mg/day; 50% of the Lovastatin () treated participants were titrated to 40 mg/day at Week 18. Of the 18 participants on Lovastatin () with consecutive elevations of either ALT or AST, 11 (0.7%) elevations occurred in participants taking 20 mg/day, while 7 (0.4%) elevations occurred in participants titrated to 40 mg/day. Elevated transaminases resulted in discontinuation of 6 (0.2%) participants from therapy in the Lovastatin () group (n=3,304) and 4 (0.1%) in the placebo group (n=3,301).
It is recommended that liver function tests be performed prior to initiation of therapy in patients with a history of liver disease, or when otherwise clinically indicated. It is recommended that liver function tests be performed in all patients prior to use of 40 mg or more daily and thereafter when clinically indicated. Patients who develop increased transaminase levels should be monitored with a second liver function evaluation to confirm the finding and be followed thereafter with frequent liver function tests until the abnormality(ies) returns to normal. Should an increase in AST or ALT of three times the upper limit of normal or greater persist, withdrawl of therapy with Lovastatin () is recommended.
The drug should be used with caution in patients who consume substantial quantities of alcohol and/or have a past history of liver disease. Active liver disease or unexplained transaminase elevations are contraindications to the use of Lovastatin () .
As with other lipid-lowering agents, moderate (less than three times the upper limit of normal) elevations of serum transaminases have been reported following therapy with Lovastatin () (see ). These changes appeared soon after initiation of therapy with Lovastatin () , were often transient, were not accompanied by any symptoms and interruption of treatment was not required.
Lovastatin () Precautions
Lovastatin () may elevate creatine phosphokinase and transaminase levels (see and ). This should be considered in the differential diagnosis of chest pain in a patient on therapy with Lovastatin () .
Homozygous Familial Hypercholesterolemia: Lovastatin () is less effective in patients with the rare homozygous familial hypercholesterolemia, possibly because these patients have no functional LDL receptors. Lovastatin () appears to be more likely to raise serum transaminases (see ) in these homozygous patients.
CYP3A4 Interactions
Lovastatin () is metabolized by CYP3A4 but has no CYP3A4 inhibitory activity; therefore it is not expected to affect the plasma concentrations of other drugs metabolized by CYP3A4. Potent inhibitors of CYP3A4 (below) increase the risk of myopathy by reducing the elimination of Lovastatin () .
See , and ,
Itraconazole
Ketoconazole
Erythromycin
Clarithromycin
Telithromycin
HIV protease inhibitors
Nefazodone
Large quantities of grapefruit juice (>1 quart daily)
Interactions With Lipid-lowering Drugs That Can Cause Myopathy When Given Alone
The risk of myopathy is also increased by the following lipid-lowering drugs that are not potent CYP3A4 inhibitors, but which can cause myopathy when given alone.
See ,
Gemfibrozil
Other fibrates
Niacin (nicotinic acid) (≥ 1 g/day)
In a 21-month carcinogenic study in mice, there was a statistically significant increase in the incidence of hepatocellular carcinomas and adenomas in both males and females at 500 mg/kg/day. This dose produced a total plasma drug exposure 3 to 4 times that of humans given the highest recommended dose of Lovastatin () (drug exposure was measured as total HMG-CoA reductase inhibitory activity in extracted plasma). Tumor increases were not seen at 20 and 100 mg/kg/day, doses that produced drug exposures of 0.3 to 2 times that of humans at the 80 mg/day dose. A statistically significant increase in pulmonary adenomas was seen in female mice at approximately 4 times the human drug exposure. (Although mice were given 300 times the human dose [HD] on a mg/kg body weight basis, plasma levels of total inhibitory activity were only 4 times higher in mice than in humans given 80 mg of Lovastatin () .)
There was an increase in incidence of papilloma in the non-glandular mucosa of the stomach of mice beginning at exposures of 1 to 2 times that of humans. The glandular mucosa was not affected. The human stomach contains only glandular mucosa.
In a 24-month carcinogenicity study in rats, there was a positive dose response relationship for hepatocellular carcinogenicity in males at drug exposures between 2-7 times that of human exposure at 80 mg/day (doses in rats were 5, 30 and 180 mg/kg/day).
An increased incidence of thyroid neoplasms in rats appears to be a response that has been seen with other HMG-CoA reductase inhibitors.
A chemically similar drug in this class was administered to mice for 72 weeks at 25, 100, and 400 mg/kg body weight, which resulted in mean serum drug levels approximately 3, 15, and 33 times higher than the mean human serum drug concentration (as total inhibitory activity) after a 40 mg oral dose. Liver carcinomas were significantly increased in high dose females and mid- and high dose males, with a maximum incidence of 90 percent in males. The incidence of adenomas of the liver was significantly increased in mid- and high dose females. Drug treatment also significantly increased the incidence of lung adenomas in mid- and high dose males and females. Adenomas of the Harderian gland (a gland of the eye of rodents) were significantly higher in high dose mice than in controls.
No evidence of mutagenicity was observed in a microbial mutagen test using mutant strains of Salmonella typhimurium with or without rat or mouse liver metabolic activation. In addition, no evidence of damage to genetic material was noted in an in vitro alkaline elution assay using rat or mouse hepatocytes, a V-79 mammalian cell forward mutation study, an in vitro chromosome aberration study in CHO cells, or an in vivo chromosomal aberration assay in mouse bone marrow.
Drug-related testicular atrophy, decreased spermatogenesis, spermatocytic degeneration and giant cell formation were seen in dogs starting at 20 mg/kg/day. Similar findings were seen with another drug in this class. No drug-related effects on fertility were found in studies with Lovastatin () in rats. However, in studies with a similar drug in this class, there was decreased fertility in male rats treated for 34 weeks at 25 mg/kg body weight, although this effect was not observed in a subsequent fertility study when this same dose was administered for 11 weeks (the entire cycle of spermatogenesis, including epididymal maturation). In rats treated with this same reductase inhibitor at 180 mg/kg/day, seminiferous tubule degeneration (necrosis and loss of spermatogenic epithelium) was observed. No microscopic changes were observed in the testes from rats of either study. The clinical significance of these findings is unclear.
Pregnancy Category X: See .
Lovastatin () has been shown to produce skeletal malformations in offspring of pregnant mice and rats dosed during gestation at 80 mg/kg/day (affected mouse fetuses/total: 8/307 compared to 4/289 in the control group; affected rat fetuses/total: 6/324 compared to 2/308 in the control group). Female rats dosed before mating through gestation at 80 mg/kg/day also had fetuses with skeletal malformations (affected fetuses/total: 1/152 compared to 0/171 in the control group). The 80 mg/kg/day dose in mice is 7 times the human dose based on body surface area and in rats results in 5 times the human exposure based on AUC. In pregnant rats given doses of 2, 20, or 200 mg/kg/day and treated through lactation, the following effects were observed: neonatal mortality (4.1%, 3.5%, and 46%, respectively, compared to 0.6% in the control group), decreased pup body weights throughout lactation (up to 5%, 8%, and 38%, respectively, below control), supernumerary ribs in dead pups (affected fetuses/total: 0/7, 1/17, and 11/79, respectively, compared to 0/5 in the control group), delays in ossification in dead pups (affected fetuses/total: 0/7, 0/17, and 1/79, respectively, compared to 0/5 in the control group) and delays in pup development (delays in the appearance of an auditory startle response at 200 mg/kg/day and free-fall righting reflexes at 20 and 200 mg/kg/day).
Direct dosing of neonatal rats by subcutaneous injection with 10 mg/kg/day of the open hydroxyacid form of Lovastatin () resulted in delayed passive avoidance learning in female rats (mean of 8.3 trials to criterion, compared to 7.3 and 6.4 in untreated and vehicle-treated controls; no effects on retention 1week later) at exposures 4 times the human systemic exposure at 80 mg/day based on AUC. No effect was seen in male rats. No evidence of malformations was observed when pregnant rabbits were given 5 mg/kg/day (doses equivalent to a human dose of 80 mg/day based on body surface area) or a maternally toxic dose of 15 mg/kg/day (3 times the human dose of 80 mg/day based on body surface area).
Rare clinical reports of congenital anomalies following intrauterine exposure to HMG-CoA reductase inhibitors have been received. However, in an analysis† of greater than 200 prospectively followed pregnancies exposed during the first trimester to Lovastatin () or another closely related HMG-CoA reductase inhibitor, the incidence of congenital anomalies was comparable to that seen in the general population. This number of pregnancies was sufficient to exclude a 3-fold or greater increase in congenital anomalies over the background incidence.
Maternal treatment with Lovastatin () may reduce the fetal levels of mevalonate, which is a precursor of cholesterol biosynthesis. Atherosclerosis is a chronic process, and ordinarily discontinuation of lipidlowering drugs during pregnancy should have little impact on the long-term risk associated with primary hypercholesterolemia. For these reasons, Lovastatin () should not be used in women who are pregnant, or can become pregnant (see ). Lovastatin () should be administered to women of child-bearing potential only when such patients are highly unlikely to conceive and have been informed of the potential hazards. Treatment should be immediately discontinued as soon as pregnancy is recognized.
† Manson, J.M., Freyssinges. C., Ducrocq, M.B., Stephenson, W.P., Postmarketing Surveillance of Lovastatin () and Simvastatin Exposure During Pregnancy. Reproductive Toxicology. 10(6):439-446. 1996.
Lovastatin () Adverse Reactions
Lovastatin () is generally well tolerated; adverse reactions usually have been mild and transient.
Phase III Clinical Studies: In Phase III controlled clinical studies involving 613 patients treated with Lovastatin () , the adverse experience profile was similar to that shown below for the 8,245-patient EXCEL study (see ).
Persistent increases of serum transaminases have been noted (see , ). About 11% of patients had elevations of CK levels of at least twice the normal value on one or more occasions. The corresponding values for the control agent cholestyramine was 9 percent. This was attributable to the noncardiac fraction of CK. Large increases in CK have sometimes been reported (see , ).
Expanded Clinical Evaluation Of Lovastatin () (EXCEL) Study: Lovastatin () was compared to placebo in 8,245 patients with hypercholesterolemia (total-C 240-300 mg/dL [6.2-7.8 mmol/L]) in the randomized, double-blind, parallel, 48-week EXCEL study. Clinical adverse experiences reported as possibly, probably or definitely drug-related in ≥ 1% in any treatment group are shown in the table below. For no event was the incidence on drug and placebo statistically different.
Other clinical adverse experiences reported as possibly, probably or definitely drug-related in 0.5 to 1.0 percent of patients in any drug-treated group are listed below. In all these cases the incidence on drug and placebo was not statistically different. Body as a Whole: chest pain; Gastrointestinal: acid regurgitation, dry mouth, vomiting; Musculoskeletal: leg pain, shoulder pain, arthralgia; Nervous System/Psychiatric: insomnia, paresthesia; Skin: alopecia, pruritus; Special Senses: eye irritation.
In the EXCEL study (see , ), 4.6% of the patients treated up to 48 weeks were discontinued due to clinical or laboratory adverse experiences which were rated by the investigator as possibly, probably or definitely related to therapy with Lovastatin () . The value for the placebo group was 2.5%.
Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS): In AFCAPS/TexCAPS (see , ) involving 6,605 participants treated with 20-40 mg/day of Lovastatin () (n=3,304) or placebo (n=3,301), the safety and tolerability profile of the group treated with Lovastatin () was comparable to that of the group treated with placebo during a median of 5.1 years of follow-up. The adverse experiences reported in AFCAPS/TexCAPS were similar to those reported in EXCEL (see , ).
Concomitant Therapy: In controlled clinical studies in which Lovastatin () was administered concomitantly with cholestyramine, no adverse reactions peculiar to this concomitant treatment were observed. The adverse reactions that occurred were limited to those reported previously with Lovastatin () or cholestyramine. Other lipid-lowering agents were not administered concomitantly with Lovastatin () during controlled clinical studies. Preliminary data suggests that the addition of gemfibrozil to therapy with Lovastatin () is not associated with greater reduction in LDL-C than that achieved with Lovastatin () alone. In uncontrolled clinical studies, most of the patients who have developed myopathy were receiving concomitant therapy with cyclosporine, gemfibrozil or niacin (nicotinic acid). The combined use of Lovastatin () at doses exceeding 20 mg/day with cyclosporine, gemfibrozil, other fibrates or lipid-lowering doses (≥ 1g/day) of niacin should be avoided (see , ).
The following effects have been reported with drugs in this class. Not all the effects listed below have necessarily been associated with Lovastatin () therapy.
Skeletal: muscle cramps, myalgia, myopathy, rhabdomyolysis, arthralgias.
Neurological: dysfunction of certain cranial nerves (including alteration of taste, impairment of extraocular movement, facial paresis), tremor, dizziness, vertigo, memory loss, paresthesia, peripheral neuropathy, peripheral nerve palsy, psychic disturbances, anxiety, insomnia, depression.
Hypersensitivity Reactions: An apparent hypersensitivity syndrome has been reported rarely which has included one or more of the following features: anaphylaxis, angioedema, lupus erythematous-like syndrome, polymyalgia rheumatica, dermatomyositis, vasculitis, purpura, thrombocytopenia, leukopenia, hemolytic anemia, positive ANA, ESR increase, eosinophilia, arthritis, arthralgia, urticaria, asthenia, photosensitivity, fever, chills, flushing, malaise, dyspnea, toxic epidermal necrolysis, erythema multiforme, including Stevens-Johnson syndrome.
Gastrointestinal: pancreatitis, hepatitis, including chronic active hepatitis, cholestatic jaundice, fatty change in liver; and rarely, cirrhosis, fulminant hepatic necrosis, and hepatoma; anorexia, vomiting.
Skin: alopecia, pruritus. A variety of skin changes (e.g., nodules, discoloration, dryness of skin/mucous membranes, changes to hair/nails) have been reported.
Reproductive: gynecomastia, loss of libido, erectile dysfunction.
Eye: progression of cataracts (lens opacities), ophthalmoplegia.
Laboratory Abnormalities: elevated transaminases, alkaline phosphatase, g-glutamyl transpeptidase, and bilirubin; thyroid function abnormalities.
Lovastatin () Overdosage
After oral administration of Lovastatin () to mice, the median lethal dose observed was >15 g/m2.
Five healthy human volunteers have received up to 200 mg of Lovastatin () as a single dose without clinically significant adverse experiences. A few cases of accidental overdosage have been reported; no patients had any specific symptoms, and all patients recovered without sequelae. The maximum dose taken was 5-6 g.
Until further experience is obtained, no specific treatment of overdosage with Lovastatin () can be recommended.
The dialyzability of Lovastatin () and its metabolites in man is not known at present.
Lovastatin () Dosage And Administration
The patient should be placed on a standard cholesterol-lowering diet before receiving Lovastatin () and should continue on this diet during treatment with Lovastatin () (see NCEP Treatment Guidelines for details on dietary therapy). Lovastatin () should be given with meals.
Adult Patients: The usual recommended starting dose is 20 mg once a day given with the evening meal. The recommended dosing range is 10-80 mg/day in single or two divided doses; the maximum recommended dose is 80 mg/day. Doses should be individualized according to the recommended goal of therapy (see NCEP Guidelines and ). Patients requiring reductions in LDL-C of 20% or more to achieve their goal (see ) should be started on 20 mg/day of Lovastatin () . A starting dose of 10 mg may be considered for patients requiring smaller reductions. Adjustments should be made at intervals of 4 weeks or more.
Cholesterol levels should be monitored periodically and consideration should be given to reducing the dosage of Lovastatin () if cholesterol levels fall significantly below the targeted range.
Lovastatin () How Supplied
Lovastatin () Tablets, USP are available as follows:
10 mg — Each white, round, flat faced beveled edge tablet imprinted with on one side and 633 on the other side contains 10 mg of Lovastatin () . Tablets are supplied in unit dose packages of 100 (10x10) NDC 68084-131-01.
20 mg — Each pink, round, flat faced beveled edge tablet imprinted with on one side and 634 on the other side contains 20 mg of Lovastatin () . Tablets are supplied in unit dose packages of 100 (10x10) NDC 68084-132-01.
40 mg — Each yellow, round, flat faced beveled edge tablet imprinted with on one side and 635 on the other side contains 40 mg of Lovastatin () . Tablets are supplied in unit dose packages of 100 (10x10) NDC 68084-133-01.
Lovastatin () Principal Display Panel - Mg
Lovastatin () Principal Display Panel - Mg
Lovastatin () Principal Display Panel - Mg
